A protein that helps cancer grow may also strengthen the immune system’s ability to fight it. Scientists at Cold Spring Harbor Laboratory in New York discovered that activating PPARδ in certain immune cells improved their ability to attack tumors, even though the same protein can encourage cancer growth.
The finding comes in a year when the American Cancer Society estimates 158,850 new colorectal cancer cases in the United States. While the results are promising, the approach has not been proven effective in human patients.
Published October 14 in Nature Immunology, the study was led by assistant professor Semir Beyaz. Researchers tested the protein’s effects in mice, human cancer cells, and miniature tumors grown from patient tissue.
The discovery suggests that a protein linked to cancer growth may also be a useful target for strengthening existing cancer treatments.
How One Protein Can Produce Opposite Results
Researchers found that PPARδ supports tumor growth in cancer cells but can strengthen the immune response when activated in certain immune cells.
PPARD, short for peroxisome proliferator-activated receptor delta, regulates gene activity and helps cells use fat for energy.
The team investigated whether cancer cells and immune cells depend on similar biological mechanisms to function.
“We hypothesized that the fitness determinants of cancer and our immune cells may not be so different,” Beyaz explained in Cold Spring Harbor Laboratory’s announcement.
Experiments involving colorectal cancer showed that PPARδ activation supported tumor growth in cancer cells. However, activating the protein in immune cells, particularly CD8-positive T cells, improved their ability to attack tumors.
The findings suggest that where the protein is activated may be as important as the protein itself.
Why Fat Metabolism Matters to Immune Cells
The scientists found that activating PPARδ improved how certain immune cells processed fat for energy, strengthening their performance against cancer in experimental models.
“It’s all about cell fitness,” Beyaz said. “What cells eat affects who they are. When immune cells burn more fat, they become more fit for fighting cancer.”
The researchers identified changes in fatty acid oxidation, the process through which cells break down fat to produce energy. These changes were associated with improved immune cell function.
The findings point toward a possible way to strengthen immunotherapy by changing how cancer-fighting immune cells produce and use energy.
They do not suggest that dietary changes would produce the same results.
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Engineered Immune Cells Showed Promising Results
Activating PPARδ improved engineered immune cells’ ability to attack human colorectal cancer in laboratory experiments and animal models.
The researchers tested the approach using CAR T cells, immune cells engineered to recognize and attack cancer.
Although CAR T cell therapies already treat certain blood cancers, treating solid tumors remains more difficult.
Scientists activated PPARδ in engineered human CAR T cells and tested them against colorectal cancer cell lines, patient-derived miniature tumors, and tumors implanted in mice.
In these models, the modified immune cells showed stronger anti-cancer activity, with some experiments showing slowed or stopped tumor growth.
The findings were particularly relevant to microsatellite stable colorectal cancer, a form of the disease that generally responds poorly to existing immune checkpoint treatments.
The team also investigated PPARδ activity in breast cancer, ovarian cancer, and melanoma models, expanding the discovery’s potential relevance.
A Star Wars Comparison Explains the Discovery
Image Credit: mozakim via 123RF
Beyaz compared the protein’s opposing effects to the light and dark sides of the Force in Star Wars.
“It’s the classic fight between good and evil,” Beyaz said. “How can good ultimately prevail? Activating PPARD in immune cells could be the way.”
The comparison reflects the central finding: a biological mechanism that benefits cancer cells can also support the immune system when activated in a different cellular environment.
But that contrast presents a challenge. Any future treatment would need to direct PPARδ activity toward immune cells without encouraging tumor growth elsewhere.
The study shows why this approach deserves investigation, not that scientists have already developed a safe way to use it in patients.
What Comes Next for Cancer Research
The findings suggest a possible strategy to improve immunotherapy, but important questions about safety and effectiveness remain unanswered.
The study, titled Compartment-specific PPARδ activity controls the outcome of cancer–immune cell competition and immunotherapy efficacy, was published in Nature Immunology on October 14, 2026.
Its results come from laboratory experiments and animal models. Researchers have not established whether the same approach can safely improve cancer treatment outcomes in people.
Future research must determine how selectively PPARδ can be activated in immune cells and whether the benefits observed experimentally can be reproduced in patients.
The discovery also opens a broader question about cancer treatment. Rather than targeting every biological process that helps tumors survive, researchers may find opportunities to use some of those same processes to strengthen immune defenses.
If a protein that helps cancer grow can also help immune cells fight it, could controlling where it acts become another way to improve cancer treatment?
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